This study examined the expanded definition of diagnostic criteria contributing to AUD as defined by the American Psychiatric Association’s DSM-5. Additive genetic effects are partially shared across DSM-5 symptoms of AUD, with genetic correlations > 0.80 for several criteria. However, correlations across some criteria were as low as 0.21 (e.g., craving and time spent), suggesting the possibility of a violation of the assumption of genetic homogeneity underlying the AUD phenotype, but this was not a common occurrence (i.e. percentage of correlations >0.3=98%, >0.6=78%, and >0.8=42%). Notably, while the standard errors for some of these correlation estimates was fairly large (e.g., rG=0.21 (SE=0.73) for the association between craving and ‘A great deal of time spent to obtain/use/recover from alcohol’), other correlations were more precise (e.g., rG=1.00 (SE=0.20) for ‘Recurrent use resulting in failure to fulfill major roles’ associated with ‘Given up or cut back on important activities in order to drink’), and thus, the hypothesis of underlying genetic homogeneity cannot be fully rejected. However, it is possible that the ability to localize genetic loci for AUDs is likely to be reduced
